Understanding the Effect of Cytokines on bEND.3 Cells in the Blood Brain Barrier in Neuropsychiatric Systemic Lupus Erythematosus
Neuropsychiatric systemic lupus erythematosus (NPSLE) is an autoimmune condition that can develop as a result of systemic lupus erythematosus (SLE). NPSLE can occur in between 12-90% of all people with SLE and can manifest as symptoms as insignificant as headaches or as detrimental as cognitive impairment and cognitive decline. The development of NPSLE has been attributed to the degradation of the blood brain barrier (BBB), a vascular network around the brain that mediates the movement of molecules into and out of the brain. In NPSLE the permeability of the BBB increases, allowing pro-inflammatory cytokines and other immune cells to cross into the brain, causing damage to neurons and sections of the brain. In this study, we attempted to investigate the mechanisms with which BBB breach can happen by screening serum from NPSLE patients for elevated protein biomarkers, and then using those to determine their effects on bEND.3 cells in the BBB through cytotoxicity assays. Cytokines IL-2, IL-17 and TGF-? were found to be elevated and therefore, MTT assays were used to determine the amount of cell death experienced by bEND.3 when exposed to these cytokines for different periods of time. The results showed vague trends and patterns but generally remained inconclusive. On the whole, shorter exposure times and lower concentrations of cytokines induced greater cell death. In some cases, results exhibited cell proliferation instead of cell death, by having cell viability percentages larger than that of the untreated control. Flow cytometry revealed the bEND.3 cells had been contaminated by RAW 264.7 macrophages, shedding light on the nature of the strange results. While the results on the effect of cytokines on bEND.3 remains inconclusive, the data presents some possibilities about the role of cytokines in cell proliferation of immune cells.